Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020672 (hypothermia)
 17,327 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

1. The aim of this investigation was to determine whether supersensitivity of isolated atria to sympathomimetic amines following pretreatment with reserpine was evident at low temperatures, which alone induced supersensitivity. 2. Cumulative dose-response curves for the positive inotropic and chronotropic responses of isolated guinea-pig atria to isoprenaline and the partial agonist salbutamol were plotted as a percentage of the maximum response to isoprenaline. 3. In atria from reserpine-pretreated guinea-pigs set up at 38 degrees C, supersensitivity of both rate and tension responses was observed as a shift of the curves to the left and an increase of the maximum responses to salbutamol. Tension responses were potentiated more than rate responses. At 30 degrees C the supersensitivity became less apparent and at 25 degrees C was virtually absent. 4. The dose-response curves in untreated atria at low temperatures revealed that hypothermia itself produced supersensitivity of rate and tension responses. The dose-response curves were displaced to the left and the salbutamol maxima were raised so that at 25 degrees C it became almost a full agonist. The hypothermia-induced supersensitivity was therefore sufficient to mask any supersensitivity resulting from pretreatment with reserpine. 5. The hypothermia-induced supersensitivity of the rate response was dependent upon the method of plotting. When plotted in absolute units of beats per min no supersensitivity of the rate response was evident. Supersensitivity of the tension response at the lower temperatures and of both rate and tension responses following pretreatment with reserpine were independent of the plotting method.
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PMID:The influence of temperature upon reserpine-induced supersensitivity of guinea-pig isolated atria to isoprenaline and salbutamol. 85 68

Ischemia of the myocardium results in a loss of ultrastructure and function. Tension generation is diminished or abolished, electrolyte imbalance occurs, and the ATP-generating capacity of the mitochondria is reduced. An intracellular accumulation of Ca2+ appears to precipitate many of these changes, the intracellular accumulation of Ca2+ being caused, in turn, by a failure of the ATP-dependent mechanisms responsible for maintaining intracellular homeostasis with respect to Ca2+. This hypothesis has been tested by the use of hypothermia, pretreatment with verapamil and a reduced extracellular Ca2+ to modify the events precipitated by an ischemic episode.
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PMID:The role of calcium in the ischemic myocardium. 700 22